靶向NETO2可抑制肝细胞癌的细胞增殖、侵袭和迁移,并使STAT3/C-MYC通路失活。

IF 2.5 3区 医学 Q3 ONCOLOGY
Na Shun Meng He, Xinghua Wu, Shu Chen, Xinyi Yun, Shun Yao, Hai Yu
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引用次数: 0

摘要

背景:Neuropilin和tolloloid - 2 (NETO2)促进多种癌症的进展,但其在肝细胞癌(HCC)中的作用尚不清楚。本研究旨在评估靶向NETO2在HCC中的潜力及其与STAT3/C-MYC通路的关系。方法:培养HCC细胞(Huh7和MHCC-97 H),转染对照siRNA (siCtrl)、NETO2 siRNA (siNETO2)、对照过表达(oeCtrl)或NETO2过表达(oeNETO2),未转染细胞作为空白对照。结果:NETO2 mRNA和蛋白在Huh7和MHCC-97 H细胞中的表达均降低。EdU和CCK-8检测显示,转染sinineto2后,Huh7和MHCC-97 H细胞的增殖能力下降。TUNEL检测发现,转染siNETO2后MHCC-97 H细胞的细胞凋亡率更高,转染Huh7细胞的细胞凋亡率更高(但差异无统计学意义)。Transwell侵袭实验显示,转染siNETO2后,Huh7和MHCC-97 H细胞的侵袭数量减少。细胞划痕实验显示,转染siNETO2后,Huh7细胞的细胞迁移率降低,而MHCC-97 H细胞的细胞迁移率无显著差异。Western blotting结果显示,转染sinineto2后,Huh7和MHCC-97 H细胞中p-STAT3和C-MYC的表达降低。过表达实验显示,转染oeNETO2后,Huh7和MHCC-97 H细胞增殖和侵袭能力增强,但细胞凋亡率降低。结论:NETO2敲低可抑制HCC细胞的增殖、侵袭和迁移,并使STAT3/C-MYC通路失活,提示NETO2是HCC治疗的潜在靶点。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Targeting NETO2 suppresses cell proliferation, invasion, and migration and inactivates the STAT3/C-MYC pathway in hepatocellular carcinoma.

Background: Neuropilin and tolloid-like 2 (NETO2) facilitates the progression of various cancers, but its role in hepatocellular carcinoma (HCC) is not known. This study aimed to assess the potential of targeting NETO2 in HCC and its relationship with the STAT3/C-MYC pathway.

Methods: HCC cells (Huh7 and MHCC-97 H) were cultured and transfected with control siRNA (siCtrl), NETO2 siRNA (siNETO2), control overexpression (oeCtrl), or NETO2 overexpression (oeNETO2), with non-transfected cells used as blank controls.

Results: NETO2 mRNA and protein expressions were reduced in both Huh7 and MHCC-97 H cells. EdU and CCK-8 assays indicated that cell proliferation was decreased after siNETO2 transfection in Huh7 and MHCC-97 H cells. TUNEL assay found revealed that the cell apoptosis rate was greater after siNETO2 transfection in MHCC-97 H cells, and tended to be greater in Huh7 cells (but the difference was not statistically significant). Transwell invasion assay revealed that the number of invasive Huh7 and MHCC-97 H cells decreased after siNETO2 transfection. Cell scratch assay revealed that the cell migration rate was reduced after siNETO2 transfection in Huh7 cells but was not significantly different in MHCC-97 H cells. Western blotting revealed that p-STAT3 and C-MYC expressions were decreased after siNETO2 transfection in Huh7 and MHCC-97 H cells. Overexpression experiments revealed that cell proliferation and invasion were promoted but that the cell apoptosis rate was reduced after oeNETO2 transfection in Huh7 and MHCC-97 H cells.

Conclusion: NETO2 knockdown suppresses HCC cell proliferation, invasion, and migration and inactivates the STAT3/C-MYC pathway, suggesting that NETO2 is a potential target for HCC treatment.

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来源期刊
CiteScore
4.70
自引率
15.60%
发文量
362
审稿时长
3 months
期刊介绍: World Journal of Surgical Oncology publishes articles related to surgical oncology and its allied subjects, such as epidemiology, cancer research, biomarkers, prevention, pathology, radiology, cancer treatment, clinical trials, multimodality treatment and molecular biology. Emphasis is placed on original research articles. The journal also publishes significant clinical case reports, as well as balanced and timely reviews on selected topics. Oncology is a multidisciplinary super-speciality of which surgical oncology forms an integral component, especially with solid tumors. Surgical oncologists around the world are involved in research extending from detecting the mechanisms underlying the causation of cancer, to its treatment and prevention. The role of a surgical oncologist extends across the whole continuum of care. With continued developments in diagnosis and treatment, the role of a surgical oncologist is ever-changing. Hence, World Journal of Surgical Oncology aims to keep readers abreast with latest developments that will ultimately influence the work of surgical oncologists.
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